Manipulation of central serotin (5HT) activity are among the most common pharmacological treatments for psychiatric, including depression and anxiety. These treatments enhance brain serotin activity either by promoting the synthesis and release of 5HT (e.g., fenfluramine) or by potenting 5HT activity in the synaptic junction between neurons (e.g., the selective-serotine reuptake inhibitors). Although the effects of these commonly used 5HT agonists on emotional processes widely explored in humans. Data from a preliminary study suggests that augmentation of central serotonin release by fenfluramine results in impaired working memory function in normal adults. Such neurocognitive effects are important to identify in order to better-understand (a) the overall neurobehavioral profile of commonly used therapeutic agents, and (b) the neurophysiological bases of congnition and emotion in healthy versus emotionaly-disordered individuals. This study proposes to address these issues by prospectively measuring cognitive and emotional changes in normal individuals following acute tryptophan depletion, placebo, and acute tryptophan augmentation.